During heavy resistance exercise extremely high MAPs are possible (MacDougall et al. 1985) with these pressures exceeding the proposed autoregulatory upper limit (Lassen 1959; Tan
168 2012). Despite the progressive increases in MAP experienced at greater loads during the effort, MCAv remained unchanged. Whilst MCAv did increase from baseline with all loads, which reflects the high-pass filter characteristics of the cerebral circulation (Zhang et al. 1998a), there was no difference between loads. If indeed the cerebral circulation is a high pass filter then a larger transient MAP increase would expected to be translated un-buffered with a large MCAv increase apparent. Given the magnitude of the MAP increases, elevated sympathetic tone in the cerebral vessels cannot be excluded (Cassaglia et al. 2008). However, due to the MAP profile and the speed of the increases a more mechanical effect may be apparent. The results from Chapter Five indicated that the VM may be responsible for this potential restraint of MCAv at the highest load (90% 6RM). The rapid translation of intrathoracic pressure to the cerebral circulation and subsequently elevations in ICP could explain this restraint. This was tested experimentally in Chapter Six, and again,despite the increasing MAP with the relative intensity of the VM, MCAv remained unchanged.
Recruitment of the VM is obligatory above 80% of the MVC (MacDougall et al. 1992) and is in agreement with the data presented in Chapter Five as the VM was only recruited at the greatest load. Recruitment of the VM does exacerbate the MAP response during resistance exercise (Pott et al. 2003), although despite this dramatic increase in MAP, MCAv is restrained. The reduction in transmural pressure of the cerebral arteries (Haykowsky et al. 2003) in response to changes in ICP (Greenfield et al. 1984) may limit the dilation of the cerebral vessels in response to increases in perfusion pressure. Although CPP is also dependent on venous outflow pressure, the internal jugular veins collapse in the standing position (Gisolf et al. 2004a) which take some time to distend during a VM (Pott et al. 2000) and is therefore only likely to have an effect after a significant increase in venous pressure
169 has been established for some time. At least initially the restraint occurs possibly through the reduction in transmural pressure, however as central venous and/or cerebrospinal fluid/Intracranial pressure was not measured this remains speculative. The maintenance of a high venous outflow pressure and ICP will have a pronounced effect on cerebral blood flow in the face of a declining MAP as seen during phase II of the VM. So whilst the elevated ICP may restrain MCAv during phase I and be potentially positive, as the VM progresses this maintained resistance to flow as MAP declines may contribute to cerebral hypoperfusion/syncope. Throughout all the experiments presented in this thesis MAP is reported as a reflection of CPP, in reality in the standing position CPP is likely to be lower because of the physical distance between the cerebral circulation and the heart. Thus, some caution must be made when comparing the reported absolute MAP and the pressure at the cerebral circulation. Regardless of this it appears that irrespective of the MAP response to either the VM in isolation or in combination with resistance exercise, the VM appears to be protective in combating large increases in MAP, despite actually contributing to this increase.
Immediately following resistance exercise and during phase III of a VM a large hypotension was seen with subsequent cerebral hypoperfusion. In both instances the hypotension appears to be posture dependent. Previous experiments utilising a leg-press movement, after which the participants remained seated (Edwards et al. 2002) or stood following exercise (Romero & Cooke 2007), resulted in smaller reductions in MCAv (both absolute change and values) than reported in Chapter Five. However it should be noted that VMs were not performed in these previous studies which would contribute to the hypotension and subsequent reduction in MCAv. Further, previous work has shown that when a VM is
170 performed whilst supine (i.e., similar to the leg-press movement) the phase III reduction in MCAv is minimal (Tiecks et al. 1995b; Pott et al. 2000). Thus, the effects of the phase III response to the VM is highly posture dependent as syncope was observed in several participants during standing VMs in Chapter Six. The added circulatory stress from orthostasis results in a greater hypotension and cerebral hypoperfusion following resistance exercise and during phase III of the VM. Although this was not formally addressed in this thesis, when comparing the current data with that previously published the effect of posture is evident. Therefore, the results of Chapters Five and Six demonstrate that in healthy resistance trained males the VM is protective against acute dynamic changes in MAP during upright resistance exercise and during the strain of a VM. However, dynamic changes in MAP are reflected proportionately by changes in MCAv following resistance exercise and release of the VM (phase III). This demonstrates that the VM both contributes and challenges cerebral regulation.
A potential limitation of the experiments presented in Chapters Five and Six was that dynamic cerebral autoregulation was not formally assessed. Although the primary aim of this thesis was not to assess dynamic cerebral autoregulatory efficacy, its quantification does have implications for the results presented within the experimental chapters and therefore requires comment. Although there are several ways of defining the dynamic autoregulatory relationship between changes in MAP and MCAv, many are problematic and assume a simplistic relationship (Tzeng & Ainslie 2013). Indeed, transfer function analysis does describe the dynamic relationship between the arterial blood pressure (input) and MCAv (output) and their linear dependence upon each other (coherence) (Zhang et al. 1998a). Also, using this analysis technique the relative magnitude (gain) and timing (phase)
171 of changes between the input and output can be determined (Zhang et al. 1998a). However, the relationship between these variables does not appear to be linear (Tan 2012; Tan et al. 2013; Tan & Taylor 2014), with differential efficacies between the hypo- and hypertensive ranges (Tzeng et al. 2010b). Furthermore, the efficacy of dynamic regulation is dependent on PaCO2 (Aaslid et al. 1989). Transfer function analysis, along with non-linear analyses such
as project pursuit regression (Tan 2012), require oscillatory changes in MAP at varying frequencies that are larger than that at resting as these analyses determine efficacy within the frequency domain. Accordingly, the results of such analyses are difficult to determine and often present conflicting results (Tzeng & Ainslie 2013). Also, a large recording of data is required to conduct this analysis (>30 s up to 5 min). As the perturbations utilised in
Chapters Five and Six were of such a short duration this method of analysis would not have
been appropriate. Whilst a disturbance in cerebral autoregulation has been reported following semi-recumbent resistance exercise these data were collected during 30 s following the effort (Koch et al. 2005). More importantly the changes in cerebrovascular resistance and MCAv pulsatility were conflicting and mimicked those at syncope (Koch et al. 2005), and thus are in agreement with the results in Chapter Five. However, as the data were taken over the 30 s post exercise, and the participants remained semi-recumbent, no reduction in MAP or MCAv was reported and thus the results are difficult to compare.
The VM can also be used to assess the efficacy of dynamic cerebral autoregulation in patients (Tiecks et al. 1996) and in healthy individuals (Tiecks et al. 1995b) by comparing the changes in MAP and MCAv between the distinct phases within phase II. Whilst MAP and subsequently MCAv are reduced during phase II when performed in isolation, syncope occurred in Chapter Six upon the release of the manoeuvre (phase III). Accordingly, phase II
172 was not the focus in this thesis. Due to the nature of the resistance exercise utilised in
Chapter Five (short dynamic efforts), length of VMs (short ~2 s) performed and the elevated
MAPs, phase II (either a or b) of the VM was not discernible. Therefore, these types of autoregulatory quantification were not conducive to the main aims of this thesis. Moreover, syncope during phase III ultimately highlights the inadequacies of cerebral autoregulation, presumably as arterial blood pressure has decreased below the lower limit of autoregulation. As all participants were health screened before taking part and none presented with cerebral or cardiovascular pathologies normal operative cerebral autoregulatory processes were assumed. This appears to be the case in both Chapter Six
and Seven as immediately following resistance exercise and during phase III of the VM,
respectively, MCAv reached nadir before MAP and also recovered earlier. Therefore, although not formally assessed dynamic cerebral autoregulation still appears to be operative in the healthy individuals investigated in this thesis.